Pim-1 kinase promotes inactivation of the pro-apoptotic Bad protein by phosphorylating it on the Ser112 gatekeeper site.
摘要：
Constitutive expression of the Pim-1 kinase prolongs survival of cytokine-deprived FDCP1 cells, partly via maintenance of Bcl-2 expression. Here, we show that Pim-1 colocalizes and physically interacts with the pro-apoptotic Bad protein and phosphorylates it in vitro on serine 112, which is a gatekeeper site for its inactivation. Furthermore, wild-type Pim-1, but not a kinase-deficient mutant, enhances phosphorylation of this site in FDCP1 cells and protects cells from the pro-apoptotic effects of Bad. Our results suggest that phosphorylation of Bad by Pim-1 is one of several mechanisms via which the Pim-1 kinase can enhance Bcl-2 activity and promote cell survival.
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关键词：
IL, interleukin GST, glutathione S-transferase DMEM, Dulbecco's modified Eagle's medium FCS, fetal calf serum Neo, neomycin SDS, sodium dodecyl sulfate PAGE, polyacrylamide gel electrophoresis Pim-1 Kinase Bcl- 2 Bad Apoptosis Myeloid cells
DOI：
10.1016/j.febslet.2004.06.050
被引量：
年份：
2004
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